U.S. patent application number 09/931804 was filed with the patent office on 2002-05-09 for implantable stimulator systems and methods for treatment of incontinence and pain.
Invention is credited to Loeb, Gerald E., Mann, Carla M., McGivern, James P., Richmond, Frances J.R., Whitehurst, Todd K..
Application Number | 20020055761 09/931804 |
Document ID | / |
Family ID | 35061588 |
Filed Date | 2002-05-09 |
United States Patent
Application |
20020055761 |
Kind Code |
A1 |
Mann, Carla M. ; et
al. |
May 9, 2002 |
Implantable stimulator systems and methods for treatment of
incontinence and pain
Abstract
A method and system for treatment of incontinence, urgency,
frequency, and/or pelvic pain includes implantation of electrodes
on a lead or the discharge portion of a catheter adjacent the
perineal nerve(s) or tissue(s) to be stimulated. Stimulation
pulses, either electrical or drug infusion pulses, are supplied by
a stimulator implanted remotely, and through the lead or catheter,
which is tunneled subcutaneously between the stimulator and
stimulation site. For instance, the system and method reduce or
eliminate the incidence of unintentional episodes of bladder
emptying by stimulating nerve pathways that diminish involuntary
bladder contractions, improve closure of the bladder outlet, and/or
improve the long-term health of the urinary system by increasing
bladder capacity and period between emptying. Moreover, the system
and method allow a patient to be taught to receive one or more
patterns of neural stimulation that can be prescribed by a
physician and administered without continuous oversight by a
clinical practitioner.
Inventors: |
Mann, Carla M.; (Los
Angeles, CA) ; Whitehurst, Todd K.; (Sherman Oaks,
CA) ; McGivern, James P.; (Stevenson Ranch, CA)
; Loeb, Gerald E.; (So. Pasadena, CA) ; Richmond,
Frances J.R.; (So. Pasadena, CA) |
Correspondence
Address: |
ADVANCED BIONICS CORPORATION
12740 SAN FERNANDO ROAD
SYLMAR
CA
91342
US
|
Family ID: |
35061588 |
Appl. No.: |
09/931804 |
Filed: |
August 16, 2001 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
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09931804 |
Aug 16, 2001 |
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09642979 |
Aug 18, 2000 |
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09642979 |
Aug 18, 2000 |
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PCT/US99/14775 |
Jun 29, 1999 |
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60091762 |
Jul 6, 1998 |
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60173054 |
Dec 24, 1999 |
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Current U.S.
Class: |
607/41 |
Current CPC
Class: |
A61N 1/36071 20130101;
A61N 1/37205 20130101; A61N 1/36017 20130101; A61N 1/36007
20130101 |
Class at
Publication: |
607/41 |
International
Class: |
A61N 001/36 |
Claims
What is claimed is:
1. A method for stimulating at least one tissue affecting specific
anatomical structures of the perineum, comprising: providing a
stimulator that generates a stimulation pulse in accordance with
prescribed stimulation parameters; providing at least one of a) a
lead connected to the stimulator, which lead included at least two
electrodes and b) a catheter connected to the stimulator, which
catheter includes at least one discharge portion, whereby the
stimulation pulse is delivered to at least one tissue adjacent the
electrodes or catheter discharge portion; implanting the electrodes
and/or catheter discharge portion adjacent to the at least one
tissue of the perineum to be stimulated; implanting the stimulator
at a location remote from the at least one tissue to be stimulated;
and tunneling the lead or catheter subcutaneously to the stimulator
location.
2. The method of claim 1 wherein the stimulation pulse is an
electrical pulse.
3. The method of claim 1 wherein the stimulation pulse is a drug
infusion pulse.
4. The method of claim 1 wherein implanting the electrodes and/or
catheter discharge portion is executed with a perineal approach,
which perineal approach includes guiding an insertion tool through
the skin of the perineum and depositing the electrodes and/or
catheter discharge portion adjacent to the at least one tissue of
the perineum to be stimulated.
5. The method of claim 1 wherein implanting the electrodes and/or
catheter discharge portion is executed with a vaginal approach,
which vaginal approach includes guiding an insertion tool through
the vaginal wall and depositing the electrodes and/or catheter
discharge portion adjacent to the at least one tissue of the
perineum to be stimulated.
6. The method of claim 1 wherein implanting the electrodes and/or
catheter discharge portion is executed with a rectal approach,
which rectal approach includes guiding an insertion tool through
the anal wall and depositing the electrodes and/or catheter
discharge portion adjacent to the at least one tissue of the
perineum to be stimulated.
7. The method of claim 1 wherein the electrodes and/or catheter
discharge portion are positioned adjacent to at least one of the
pudendal nerve and a pudendal nerve branch.
8. The method of claim 1 further comprising providing a
programmable memory within the stimulator for receiving and
retaining the stimulation parameters.
9. The method of claim 1 further comprising providing a power
source within the stimulator for providing operating power to the
stimulator.
10. The method of claim 1 further comprising providing at least one
external appliance for transmitting the stimulation parameters to
the stimulator.
11. The method of claim 1 wherein said at least one tissue includes
the pudendal nerve, and wherein the method treats incontinence,
urgency, frequency, and/or pelvic pain.
12. The method of claim 1 wherein said at least one tissue includes
at least one of the dorsal nerve of the clitoris and the dorsal
nerve of the penis, and wherein the method treats urinary urge
incontinence and/or detrusor hyperreflexia.
13. The method of claim 1 wherein said at least one tissue is a
nerve that innervates at least one of the urethra and the detrusor
muscle, and wherein the method treats urinary retention.
14. The method of claim 1 wherein said at least one tissue is a
nerve that innervates at least one of the internal urethral
sphincter, the external urethral sphincter, and an intramuscular
branch of a urethral sphincter, and wherein the method treats
urinary stress incontinence.
15. The method of claim 1 wherein said at least one tissue is a
nerve that innervates at least one of the clitoris and vagina, and
wherein the method treats vaginismus, dyspareunia, anorgasmia,
and/or other female sexual dysfunctions.
16. The method of claim 1 wherein said at least one tissue is a
nerve that innervates at least one of the rectum and colon, and
wherein the method treats constipation, fecal retention an d/or
colorectal hypomotility.
17. The method of claim 1 further comprising providing at least one
sensor to sense a physical condition, and adjusting the stimulation
parameters based on the sensed condition.
18. The method of claim 17 further comprising adjusting the
stimulation parameters using at least one external appliance.
19. The method of claim 17 further comprising adjusting the
stimulation parameters using the implantable stimulator.
20. A system for stimulating at least one tissue affecting specific
anatomical structures of the perineum, comprising: a stimulator
that generates a stimulation pulse in accordance with prescribed
stimulation parameters; at least one of a) a lead connected to the
stimulator, which lead includes at least two electrodes and b) a
catheter connected to the stimulator, which catheter includes a
discharge portion, whereby the stimulation pulse is delivered to at
least one tissue adjacent the electrodes or catheter discharge
portion; means for implanting the electrodes and/or catheter
discharge portion adjacent to the at least one tissue of the
perineum to be stimulated; means for implanting the stimulator at a
location remote from the at least one tissue to be stimulated; and
means for subcutaneously tunneling the lead and/or catheter to the
stimulator location.
21. The system of claim 20 wherein the stimulator is configured to
generate an electrical stimulation pulse.
22. The system of claim 20 wherein the stimulation is configured to
generate a drug infusion stimulation pulse.
23. The system of claim 20 further comprising means for implanting
the electrodes and/or catheter discharge portion adjacent to at
least one of the pudendal nerve and a pudendal nerve branch.
24. The system of claim 20 wherein the stimulator includes a
programmable memory for receiving and retaining the stimulation
parameters.
25. The system of claim 20 further comprising a power source for
providing operating power to the stimulator.
26. The system of claim 25 wherein the power source is housed
within the stimulator.
27. The system of claim 26 wherein the power source is
rechargeable.
28. The system of claim 20 further comprising at least one external
appliance for transmitting power to the stimulator.
29. The system of claim 20 further comprising at least one external
appliance for transmitting the stimulation parameters to the
stimulator.
30. The system of claim 20 further comprising at least one sensor,
and wherein the stimulation parameters are adjusted based on the
sensed condition.
31. A method of treating patients with incontinence, urgency,
frequency, and/or pelvic pain, comprising: providing a stimulator
that generates a stimulation pulse in accordance with prescribed
stimulation parameters; providing at least one of a) a lead
connected to the stimulator, which lead includes at least two
electrodes and b) a catheter connected to the stimulator, which
catheter includes a discharge portion whereby the stimulation pulse
is delivered to at least one tissue adjacent the electrodes or
catheter discharge portion; perineally or vaginally implanting the
electrodes and/or catheter discharge portion adjacent to at least
one tissue to be stimulated; implanting the stimulator at a
location remote from the at least one tissue to be stimulated; and
tunneling the lead and/or catheter subcutaneously to the stimulator
location.
32. The method of claim 31 wherein the at least one tissue to be
stimulated includes at least one of a periurethral muscle, urethral
sphincter, anal sphincter, pudendal nerve, clitoral branch of the
pudendal nerve, penile branch of the pudendal nerve, inferior
rectal branch of the pudendal nerve, urethral branch of the
pudendal nerve, pelvic nerve, and pelvic floor nerves.
33. The method of claim 32 wherein the stimulation is delivered at
less than about 50 to 100 Hz.
34. The method of claim 31 wherein the at least one tissue
comprises at least one of the somatic nerves that originate from
the sacral nerve roots.
35. The method of claim 34 wherein the at least one tissue
comprises at least one of the pudendal nerve and a pudendal nerve
branch.
36. The method of claim 31 wherein the at least one implantable
stimulator further comprises at least one sensor.
37. The method of claim 36 further comprising sensing a condition
using the at least one sensor and adjusting the stimulation
parameters based on the sensed condition.
38. The method of claim 37 further comprising performing the
parameter adjustment using at least one external appliance.
39. The method of claim 37 further comprising performing the
parameter adjustment using the implantable stimulator.
Description
[0001] This application is a continuation-in-part (CIP) of
copending U.S. patent application Ser. No. 09/642,979, filed Aug.
18, 2000, which in turn is a CIP of PCT Patent application Ser. No.
PCT/US99/14775, filed Jun. 29, 1999, which in turn claims priority
to, and the benefit of, prior U.S. patent application Ser. No.
60/091,762, filed Jul. 6, 1998. U.S. patent application Ser. No.
09/642,979 also claims the benefit of U.S. patent application Ser.
No. 60/173,054, filed Dec. 24, 1999. The above-listed applications
are incorporated herein by reference.
FIELD OF THE INVENTION
[0002] The present invention relates to implantable stimulator
systems, and more particularly to an implantable stimulator system
utilizing one or more implantable stimulators for treating
incontinence and/or pain.
BACKGROUND OF THE INVENTION
[0003] Urinary incontinence is a clinical condition characterized
by failure to hold urine in the bladder under normal conditions of
pressure and filling. Urinary incontinence afflicts an estimated 13
million Americans. A 1980 British postal survey of 22,430 people
showed a prevalence of urinary incontinence of 8.5% in women and
1.6% in men aged 15-64, and 11.6% in women and 6.9% in men aged 65
and over.
[0004] Six of every seven adult incontinence cases occur in women;
15% to 30% of women experience incontinence during their lifetimes.
Women are more at risk than men because of pelvic nerve trauma
during childbirth and the comparative shortness of the female
urethra (around two inches versus ten in men). Women who have their
first child when over age 30 or who use the drug oxytocin for
inducing labor appear to be at increased risk for urinary
incontinence later on. (Such medically-induced labor tends to
subject pelvic muscles and nerves to greater forces than does
natural labor.) In addition, women who perform high-impact
exercise, such as gymnasts, and softball, volleyball, and
basketball players, are susceptible to urinary leakage,
particularly those with a low foot arch, which, on impact,
increases the shock to the pelvic area. In addition, a study of 600
women found that smokers and former smokers are twice as likely to
develop incontinence than are women who never smoked. According to
one 1999 study, urge incontinence is more common among older
postmenopausal women who are diabetic or who reported two urinary
tract infections within the past year. Obesity is also a major
factor for incontinence in older women.
[0005] Forms of Urinary Incontinence
[0006] The most common forms of urinary incontinence can arise from
either a failure of muscles around the bladder neck and urethra to
maintain closure of the urinary outlet (so-called stress
incontinence) or from abnormally heightened commands from the
spinal cord to the bladder that produce unanticipated bladder
contractions (so-called urge incontinence). Patients with stress
incontinence experience minor leakage from activities that apply
pressure to a full bladder, such as coughing, sneezing, laughing,
running, lifting, or even standing. People with urge incontinence
(also called hyperactive or irritable bladder) need to urinate
frequently or are unable to reach the bathroom before leakage. When
the bladder reaches capacity, the nerves appropriately signal the
brain that the bladder is full, but the urge to void cannot be
voluntarily suppressed--even temporarily. In a variant type of urge
incontinence called reflex incontinence, the sensation of fullness
is not adequately communicated to the brain, and in the absence of
the brain's inhibition of this automatic process, the bladder
releases urine.
[0007] Another common form of the disorder is overflow
incontinence, which results when the bladder cannot empty
completely, generally because of a partial obstruction or an
inactive bladder muscle. In contrast to urge incontinence, the
bladder is less active than normal. It cannot empty properly and so
becomes distended. Eventually this distention stretches the
internal sphincter until it opens partially and leakage occurs.
Functional, or environmental, incontinence encompasses a variety of
conditions in which the patient is unable to use the bathroom
because of physical or emotional impairments. Approximately 40% of
incontinence patients fall into more than one of these four
categories (stress, urge, overflow, and functional incontinence),
and experience so-called mixed incontinence.
[0008] Anatomy and Physiology of the Lower Urinary Tract
[0009] The urinary bladder is composed of smooth muscle
collectively referred to as the detrusor muscle. Smooth muscle of
the urethra is contiguous with the detrusor muscle and is referred
to as the internal urethral sphincter, although it is not a true
anatomic sphincter. Skeletal muscle surrounding the urethra is
called the external urethral sphincter.
[0010] Innervation of the lower urinary tract is complex. Tight
junctions between bladder smooth muscle cells allow for
transmission of nerve impulses from cell to cell. The hypogastric
nerve, originating from spinal cord segments of L1 through L4,
supplies sympathetic innervation to the bladder and urethra. The
pelvic nerve, originating from the spinal cord segments S1 through
S3, supplies parasympathetic (cholinergic) innervation to the
detrusor muscle and transmits sensory impulses from the bladder.
Somatic innervation of the muscle of the external urethral
sphincter is distributed via the pudendal nerve, originating from
spinal cord segments S1 through S3. The pudendal nerve also
innervates muscles of the anal sphincter and perineal region, and
it also transmits sensation from the perineal region and the
urethral and anal sphincters.
[0011] The sympathetic and somatic nervous systems dominate the
storage phase of micturition. Sympathetic stimulation of
beta-adrenergic receptors in the detrusor muscle results in bladder
relaxation to accommodate filling. Sympathetic stimulation of
alpha-adrenergic receptors in the neck of the bladder and internal
urethral sphincter maintains continence. Sympathetic pathways also
inhibit parasympathetic bladder innervation during storage.
Stimulation of the pudendal nerve results in increased tone of the
external urethral sphincter, contributing to continence. When the
bladder is full, sensation is transmitted via the pelvic nerve to
the sacral spinal cord, and subsequently the brainstem. Voluntary
control of urination originates from the cerebral cortex. The
storage phase of the urinary bladder can be switched to the voiding
phase either voluntarily or involuntarily (reflexively).
[0012] Signals to the cortical center generally occur when bladder
volume has reached 250 mL to 300 mL. When urination is desired,
neural impulses from the cortex are transmitted through the spinal
cord and pelvic nerves to the detrusor muscle. Daytime emptying of
the bladder may occur as often as every few hours or as
infrequently as every 8 to 12 hours. During the emptying phase of
micturition, parasympathetic (cholinergic) activity of the pelvic
nerves causes the detrusor muscle to contract and the bladder to
empty. Simultaneous inhibition of sympathetic and somatic
stimulation of the urethral smooth and skeletal muscle results in
urethral relaxation. Following complete emptying of the bladder or
voluntary cessation of urination, the storage phase begins again.
External urethral sphincter tone can increase in response to sudden
increases in abdominal pressure (e.g., during coughing) to maintain
continence. Disruption of tight junctions, peripheral nerves,
spinal cord segments, or higher brain centers may alter
micturition.
[0013] Reflex Arcs in the Lower Urinary Tract
[0014] The function of the lower urinary tract is modulated by
several reflex arcs. The most prominent of these is a positive
feedback reflex that modulates micturition. Mechanoreceptors in the
bladder are distended when the bladder is at capacity, and they
trigger a coordinated micturition reflex via a center in the upper
pons and perhaps through a spinal reflex as well. The bladder
contracts, causing an even greater distention of the
mechanoreceptors, leading to even greater activation of the
micturition reflex and bladder contraction. This ensures that the
bladder is completely emptied during normal voiding.
[0015] Other lower urinary tract reflexes are inhibitory. The
external urethral sphincter is reflexively activated by
mechanoreceptors during bladder filling, so that sphincter pressure
increases as needed. Anal dilatation has been demonstrated to
reflexively inhibit detrusor contraction, thereby preventing
involuntary urine leakage during defecation. Gentle mechanical
stimulation of the genital and perineal regions also reflexively
inhibits detrusor contraction, thereby preventing involuntary urine
leakage during sexual stimulation and coitus. The afferent portions
of these reflex arcs are carried by the pudendal nerve, which
carries somatic sensory information from the pelvic floor, and the
pelvic nerve, which carries much of the pelvic visceral sensations.
Bladder contraction is also reflexively inhibited by the activation
of stretch fibers in pelvic and limb muscles, thereby preventing
involuntary urine leakage during physical activity.
[0016] Neurologic Causes of Incontinence
[0017] Urinary incontinence may be associated with neurologic
disease. Neurologic abnormalities may disrupt the detrusor muscle,
urethral sphincters, or both. Neurologic incontinence may result
from trauma, tumors, or herniated intervertebral discs. The
location of the lesion will dictate the type of micturition
disorder and other concurrent neurologic abnormalities.
[0018] Patients with upper motor neuron (UMN) lesions--those above
the sacral spinal cord segments--lack voluntary control of
micturition. Urination may be initiated by spinal reflexes, but an
absence of sensation and central nervous system control, and the
failure of the sphincters to relax, leads to interrupted,
involuntary, and/or incomplete voiding. Manual bladder expression
is difficult if sphincter hypertonia is present, but the urethra
can be catheterized normally. Overflow of urine occurs when the
bladder pressure exceeds sphincter resistance. The perineal reflex
is intact.
[0019] Detrusor instability (a.k.a. detrusor areflexia) with
decreased sphincter tone results from disease of sacral spinal cord
segments or bilateral lesions of the sacral spinal nerve roots
(i.e., lower motor neuron, or LMN, lesions). Voluntary control of
urination is absent. Fecal incontinence may also be present, and
perineal reflexes may be absent. Detrusor instability may also
occur secondary to prolonged overdistention of the bladder. Tight
junctions between muscle cells are disrupted, preventing spread of
nerve impulses. The patient will attempt to void because sensory
pathways are intact, but the atonic, flaccid bladder is unable to
contract. Residual urine volume is large.
[0020] Reflex dyssynergia occurs with incomplete spinal cord
lesions cranial to the sacral spinal cord segments. The detrusor
reflex is normal to hyperactive, and the urethral sphincters are
hyperactive. The patient voluntarily initiates urination, but the
urine stream is abruptly stopped because there is synchronization
between bladder contraction and urethral relaxation, leading to
incomplete voiding. Urethral obstruction can result in a similar
pattern of micturition. Cerebral lesions may also result in the
loss of voluntary control of micturition.
[0021] Causes of Urge Incontinence
[0022] The most common cause of urge incontinence is detrusor
instability, where patients have involuntary detrusor contractions
that are non-neuropathic or of unknown origin. There is no general
consensus regarding the cause of detrusor instability although both
a myogenic and neurologic basis have been suggested.
[0023] Detrusor instability occurs in about 75% of men with benign
prostatic hyperplasia and causes frequency, urgency, and urination
during the night, although incontinence itself occurs only in very
severe cases. Surgical procedures, such as prostatectomy and
transurethral resection of the prostate (TURP), can cause detrusor
instability. Incontinence rates in TURP are very low (about 1%) but
they can be significant after prostatectomy. (In the latter case,
detrusor instability is usually only one of many factors involved
in incontinence.)
[0024] The other common cause of overactive bladder muscle
abnormalities and urge incontinence is detrusor hyperreflexia.
Involuntary detrusor contractions caused by detrusor hyperreflexia
may result from a central nervous system (CNS) impaired by known
neurologic conditions such as stroke, multiple sclerosis, spinal
cord or disk injury, dementia, or Parkinson's disease. These
conditions can result in detrusor hyperactivity by interfering with
the normal flow of nerve messages between the urinary system and
the CNS.
[0025] Urge incontinence results from bladder contractions that
overwhelm the ability of the cerebral centers to inhibit them.
These uncontrollable contractions can occur because of inflammation
or irritation of the bladder from calculi, malignancy, infection,
atrophic vaginitis, or urethritis. Drugs that may cause or
contribute to urge incontinence include diuretics and caffeine
(which increase urine flow), sedative hypnotics or narcotics (which
depress micturition centers in the brain), and alcohol (which also
inhibits micturition centers in the brain and has a diuretic
effect). Uncontrollable contractions can also occur when brain
centers that inhibit contractions are inhibited by metabolic
disorders such as hypoxemia and encephalopathy. Anxiety and normal
aging can also cause the bladder to become overactive. Some
evidence suggests that some cases are caused by ischemia (blockage
of blood vessels), the same process that leads to coronary artery
disease.
[0026] Disorders of the cortex may result in an overactive bladder.
Functional brain scanning in healthy volunteers during micturition
has demonstrated that specific areas of the frontal cortex may be
involved in the micturition process. These areas have demonstrated
reduced activity in elderly patients with urge incontinence.
[0027] Pathophysiology of Urge Incontinence
[0028] In a number of patients with urgency, frequency, and/or urge
incontinence, the pathological process may somehow be initiated by
a sustained or prolonged nociceptive signal via the somatic and/or
visceral afferents (due to an underlying process such as myofascial
pain or endometriosis). A prolonged nociceptive signal is believed
to cause biochemical and neuropathic changes within the spinal
cord, perhaps through reflexive activity within the bladder and
other pelvic tissues. This process has been referred to as
neurogenic inflammation, in which a neuroinflammatory process is
believed to be mediated by release of vasoactive peptides such as
substance P and neurokinin A.
[0029] "Neurogenic inflammation is the process whereby stimulation
of peripheral nerves elicits vasodilatation, plasma extravasation,
and other inflammatory changes in the skin or viscera. Neurogenic
inflammation can be evoked in the bladder by antidromic stimulation
of visceral afferents in the pelvic nerve. Although bladder
afferents relay information to the central nervous system, they
also act in the periphery to alter mucosal permeability, smooth
muscle contractility, local blood flow and to influence cellular
mediators of the immune system; thus an initial inflammatory event
may be reinforced by neurogenic mechanisms. The resulting changes
in neural processing affect the pain pathways in particular, and
perturbations in the function of peripheral and central elements of
the nociceptive system can be durable, outlasting the initial
inflammation." [Steers W D; Tuttle J B. "Chapter 8: Neurogenic
Inflammation and Nerve Growth Factor: Possible Roles in
Interstitial Cystitis", in Sant G R, ed., Interstitial Cystitis,
Lippincott Williams & Wilkins, 1997.]
[0030] With changes in spinal reflexes and the "centralization of
pain," the neuropathic changes within the spinal cord become so
pronounced that even with the removal of external insult, e.g.,
treatment of endometriosis, the neuropathic dysregulation persists.
This neuropathic change explains why patients with a chronic pelvic
pain syndrome may present with multiple overlapping symptoms that
frequently involve pelvic pain, urgency/frequency syndrome, urge
incontinence, fecal incontinence, functional bowel disease,
dyspareunia, vestibulitis, and/or dysfunctional voiding.
[0031] Current Treatments
[0032] There are many surgical procedures for urinary incontinence;
most are designed so pressure is exerted effectively at the neck of
the bladder. The four primary procedures are retropubic suspensions
(about 80% cure rate), transvaginal suspensions (60-70% cure rate),
sling procedures (about 80% cure rate), and anterior repairs
(60-70% cure rate). Suspensions have higher complication rates than
the other procedures. Studies reported by the American Urological
Association indicated that surgery should be considered as initial
therapy for women with severe stress incontinence and that surgery
is an effective and safe alternative when other treatments fail.
Potential complications of all of these surgical procedures include
obstruction of the outlet from the bladder, which causes difficulty
in urination and irritation. Surgery is typically not performed in
individuals with urge incontinence who have uninhibited bladder
contractions.
[0033] Injections of bulking materials that help support the
urethra are proving to be beneficial for people with severe stress
incontinence caused by dysfunctional sphincter muscles in the
urethra, but who still have good pelvic muscle support and
functional bladders. The bulking agent most commonly used today is
collagen, specifically animal collagen (Contigen). The collagen is
injected into the tissue surrounding the urethra. The injected
collagen tightens the seal of the sphincter by adding bulk to the
surrounding tissue.
[0034] It is well known in the art that electrical stimulation in
the region of the pelvic floor can decrease the severity of
incontinence. The improvement is believed to be attained through at
least three mechanisms: (1) by changing the reflex thresholds of
the bladder muscles responsible for bladder emptying, (2) by
strengthening the muscles that maintain closure on the bladder
outlet, and (3) by changing the state of the neural pathways,
musculature and/or bladder during and beyond the period of stimulus
application.
[0035] The electrical stimulation therapies currently available for
incontinence have generally been directed at improving muscle
condition, as disclosed, e.g., in applicant's prior document
WO97/18857 (PCT/US96/18680), published May 29, 1997. Bladder
hyperreflexia and detrusor instability have proven more difficult
to treat. However, evidence in the art suggests that it can be
improved in many individuals by stimulating peripheral nerves or
nerve roots continuously or intermittently to modulate transmission
of excitatory nerve signals to the bladder muscles.
[0036] Several external and implantable approaches have been used
to stimulate the nerves supplying the bladder and pelvic region in
order to decrease the episodic incidences of unintentional bladder
emptying. The approaches that strengthen periurethral muscles have
usually employed vaginal or anal electrode assemblages to stimulate
muscle contractions repeatedly. These methods are limited in their
portability and are often poorly accepted by patients because they
are inconvenient and often associated with unpleasant skin
sensations. Further, the methods are inadequate for the treatment
of urge incontinence in which continual electrical stimulation is
commonly needed to diminish or inhibit the heightened reflexes of
bladder muscles.
[0037] For the treatment of urge incontinence, surgically implanted
stimulators under battery or radio-frequency control have been
described in the art. These stimulators have different forms, but
are usually comprised of an implantable control module to which is
connected a series of leads that must be routed to nerve bundles in
either the sacral roots emanating from the spinal cord, or the
nerves supplying muscles, skin or other structures in the pelvic
region. The implantable devices are relatively large, expensive and
challenging to implant surgically. Thus, their use has generally
been confined to patients with severe symptoms and the capacity to
finance the surgery.
[0038] In one study, a vaginal device employing electrical
stimulation was significantly more effective than a sham device for
patients with urge incontinence, although there was no difference
for women with stress incontinence. The Stoller Afferent Neural
Stimulator (SANS) device has been applied to stimulation of the
nerves above the ankle bone; more than 75% of mild to moderate
incontinence patients treated in this way once a week for about a
half hour reported at least 50% reduction in symptoms.
[0039] Sacral Nerve Stimulation
[0040] A sacral nerve stimulation (SNS) system (Medtronic
InterStim) is available for urge incontinence, in which a
battery-operated generator that produces electrical pulses is
implanted in the abdomen. A wire connected to it runs to the sacral
nerves in the lower back. The Sacral Nerve Stimulation Study Group
compared 34 incontinence patients receiving SNS with 42 control
patients who received standard medical therapy. (Reference Schmidt,
et al., "Sacral nerve stimulation for treatment of refractory
urinary urge incontinence. Sacral Nerve Stimulation Study Group."
Journal of Urology, August 1999; 162(2):352-7.)
[0041] At 6 months, the number of daily incontinence episodes,
severity of episodes, and use of absorbent pads were significantly
reduced in the stimulation group compared to the control group. Of
the 34 SNS patients, 16 (47%) were completely dry and an additional
10 (29%) demonstrated a greater than 50% reduction in incontinence
episodes six months after implantation. Efficacy appeared to be
sustained for 18 months. During the evaluation, the group returned
to baseline levels of incontinence when stimulation was
inactivated. Urodynamic testing confirmed that SNS did not
adversely affect voiding function. Complications included
implantable pulse generator site pain in 15.9% of the patients,
implant site pain in 19.1% and lead migration in 7.0%. Surgical
revision was required in 32.5% of patients with implants to resolve
a complication. There were no reports of permanent injury or nerve
damage.
[0042] Shaker applied SNS to 16 women and 2 men with refractory
urge incontinence. (See Shaker, et al., "Sacral nerve root
neuromodulation: an effective treatment for refractory urge
incontinence." Journal of Urology May 1998; 159(5):1516-9.) Over an
average follow-up period of 18.8 months (range 3 to 83), these
patients showed a marked reduction in leakage episodes from 6.49 to
1.98 times per 24 hours. Eight patients became completely dry and 4
had average leakage episodes of 1 or less daily. Patients also
demonstrated a decrease in urinary frequency with an increase in
functional bladder capacity. Associated pelvic pain also decreased
substantially.
[0043] The mechanism of action of sacral nerve stimulation is
unknown. The afferent somatic stimulation is believed to somehow
modulate the neural reflexes involved in micturition, thereby
inhibiting micturition. The same inhibitory action is also believed
to be responsible for the control of fecal incontinence by SNS, as
described in more detail presently. SNS leads to stimulation of one
or more sacral dorsal ganglia, which may also help control somatic
and/or visceral pelvic pain through the same mechanism of action as
spinal cord stimulation (SCS). (In SCS the non-nociceptive afferent
signals are believed to "gate" or otherwise modulate central
processing of nociceptive signals, via the gate control theory.)
SNS may also stimulate the pelvic floor musculature and may be a
form of biofeedback, enabling its use in pelvic floor
rehabilitation. During typical SNS system implantation, pudendal
nerve recruitment is targeted, and may be confirmed by contractions
in the pelvic floor.
[0044] Malouf reported on implantation of chronic SNS systems in
five women (age 41-68 years) with fecal incontinence for solid or
liquid stool at least once per week. (Reference Malouf, et al.,
"Permanent Sacral Nerve Stimulation for Fecal Incontinence." Annals
of Surgery July 2000; 232(1):143-148.) These patients were followed
up for a median of 16 months after permanent implantation. All had
incontinence, and three had urge incontinence. The cause was
scleroderma in two, primary internal sphincter degeneration in one,
diffuse weakness of both sphincters in one, and disruption of both
sphincters in one. All patients had marked improvement. Urgency
resolved in all three patients with this symptom. Passive soiling
resolved completely in three and was reduced to minor episodes in
two. Continence scores (scale 0-20) improved from a median of 16
before surgery to 2 after surgery. There were no early
complications, and there have been no side effects. One patient
required wound exploration at 6 months for local pain, and a lead
replacement at 12 months for electrode displacement. The quality of
life assessment improved in all patients. The resting pressure
increased in four patients, but there was no consistent measured
physiologic change that could account for the symptomatic
improvement.
[0045] Pudendal Nerve Stimulation
[0046] Bladder contraction and micturition may be inhibited through
a number of reflex arcs, some involving afferent fibers of the
pudendal nerve, as discussed above. Distal branches of the pudendal
nerve lead to the anal sphincter, the perineum, the urethral
sphincter, the penis (in men), the vagina (in women), the glans
penis (in men), and the clitoris (in women). Stimulation of the
pudendal afferents from the anal sphincter has been demonstrated to
inhibit bladder contraction. Similarly, stimulation of the pudendal
afferents from the dorsal nerve of the penis (in men) or the dorsal
nerve of the clitoris (in women) has been demonstrated to inhibit
bladder contraction.
[0047] In 1974, Sundin, et al. demonstrated in cats that acute
electrical stimulation of the pudendal nerve leads to detrusor
inhibition. (See Sundin, et al., "Detrusor inhibition induced from
mechanical stimulation of the anal region and from electrical
stimulation of pudendal nerve afferents: An experimental study in
cats" Investigative Urology, March 1974; 11(5):374-8.) In 1986,
Vodusek, et al. demonstrated in 8 male and 2 female patients that
stimulation of the dorsal nerve of the penis or the dorsal nerve of
the clitoris with surface electrodes led to bladder inhibition and
an increase in bladder capacity in 8 of the 10 patients. (Reference
Vodusek, et al., "Detrusor inhibition induced by stimulation of
pudendal nerve afferents" Neurourology and Urodynamics, 5, 1986,
381-9.) The authors concluded that stimulation of the pudendal
nerve afferents leads to detrusor inhibition in patients with
neurological lesions above the sacral level.
[0048] In a 1988 study of three patients with urgency, frequency,
and urge incontinence, Vodusek, et al. demonstrated that acute
percutaneous electrical stimulation of the pudendal nerve at the
ischial spine led to inhibition of bladder contraction and to a
two- to four-fold increase in bladder capacity. The
neurostimulation waveform had a frequency of 1 to 5 Hz, an
amplitude of 1 to 2 mA, and a pulse width of 200 .mu.sec.
Activation of the external urethral sphincter via the efferent
fibers of the pudendal nerve may also have played a role in the
observed increase in bladder capacity. (See Vodusek, et al.,
"Detrusor inhibition on selective pudendal nerve stimulation in the
perineum" Neurourology and Urodynamics. 6, 1988, 389-93.)
[0049] U.S. Pat. No. 4,607,639 (the '639 patent) discloses a method
for controlling bladder evacuation via electrical stimulation of
sacral roots and/or pelvic floor nerves, including the pudendal
nerve. However, this method requires, first, the arduous task of,
for example, "identifying the anatomical location and functional
characteristics of those nerve fibers controlling the separate
functions of said bladder and external sphincter." This
identification is accomplished via a sacral route. Next, separating
motor and sensory and/or somatic and autonomic nerve fibers is
taught. Again, nerve fiber separation is accomplished via a sacral
route. Additionally or alternatively to the separating of nerve
fibers, the method requires isolating nerve fibers via sectioning.
Again, nerve fibers are sectioned via a sacral route.
[0050] The '639 patent indicates that the method includes
"identifying the anatomical location of at least one nerve."
However, since one or a combination of separating, sectioning, and
stimulating at least two separate nerve fibers is described, it is
clear from a careful reading that the method taught in the '639
patent requires locating and identifying at least two separate
neural structures. For example, one of the specific procedures of
the '639 patent requires identification of both the superior
somatic nerve (which innervates the levator ani muscles) and the
inferior somatic nerve (innervating the pudendal nerve at Alcock's
canal), so that the superior somatic nerve may be sectioned and the
inferior somatic nerve may be stimulated. As another example, the
S3 sacral nerve is identified, then the ventral and dorsal roots
are surgically separated (which requires their identification), so
the ventral root alone may be stimulated. Other specific procedures
require the stimulation of at least two separate neural structures,
such as the inferior somatic nerve and the S3 ventral root
(separated from the dorsal root). Such procedures may reasonably be
expected to be more time-consuming than the identification and
stimulation of a single neural structure. The '639 patent does not
teach a method in which identification of only one neural structure
is necessary, e.g., identification of a single nerve such as the
pudendal nerve, which directly controls the function of the
external sphincter and not the bladder.
[0051] Further, all the surgical procedures described in the '639
patent are performed via a sacral approach. A plethora of pelvic
area nerves emanate from the sacral segments. Therefore,
stimulation of the neural structures targeted by the '639 patent
via a sacral route results in 1) needing to identify which nerves
to stimulate, separate, or section, and 2) the actual separating
and sectioning of physically and/or physiologically close nerve
fibers. Thus, it is not surprising that the surgical procedures of
the '639 patent are complicated by the identifying, separating, and
sectioning of multiple nerves. In addition, it is difficult or
impossible to reach portions of some nerves via a sacral approach,
such as the portion of the pudendal nerve that passes through
Alcock's canal.
[0052] Additionally, the '639 patent describes only radio-frequency
control of an implanted stimulating electrode.
[0053] Many of the therapies described above have been used to
treat pelvic pain, with the same drawbacks. For instance,
neurostimulation of the sacral nerve roots has been demonstrated to
relieve pelvic pain in patients with intractable chronic pelvic
pain. Other devices used for both incontinence and pelvic pain
require that a needle electrode(s) be inserted through the skin
during stimulation sessions. These devices may only be used
acutely, and may cause significant discomfort.
[0054] What is needed are ways to effectively use implantable
stimulators to chronically stimulate the pudendal nerve and its
branches directly, for treating incontinence and/or pelvic
pain.
SUMMARY OF THE INVENTION
[0055] The systems and methods taught in this invention include the
injection, direct implantation, endoscopic, or laparoscopic
implantation of one or more battery- or radio-frequency-powered
microstimulators beneath the skin of the perineum. The systems and
methods taught also include the injection, direct implantation,
endoscopic, or laparoscopic implantation of one or more battery- or
radio-frequency-powered microstimulators on or near the tibial
nerve. The systems and methods taught also include implantation of
other, various means for chronically stimulating the pudendal nerve
and/or its branches.
[0056] The devices are programmed using, e.g., radio-frequency
control via an external controller that can be used by a physician
to produce patterns of output stimulation pulses judged to be
efficacious by appropriate clinical testing. Such stimulation
program is retained in the device or external controller and is
transmitted when commanded to start and stop by a signal from the
patient or caregiver.
[0057] It is an object of this invention to reduce or eliminate the
incidence of unintentional episodes of bladder emptying (i.e.
incontinence) as well as other dysfunctions of perineal structures,
such as urgency and frequency, by stimulating nerve pathways that
diminish involuntary bladder contractions, improve closure of the
bladder outlet, and/or improve the long-term health of the urinary
system by increasing bladder capacity and thus, the time period
between emptying. As one example of another dysfunction of perineal
structures, it is also an object of this invention to similarly
reduce or eliminate the incidence of fecal incontinence.
[0058] Another object of this invention is to reduce or eliminate
pelvic pain by chronically stimulating nerve pathways, such as
those that derive from the sacral roots, using an implantable
neurostimulator that is implanted with a minimal surgical
procedure.
[0059] It is a further object of this invention to teach a method
whereby a patient can receive one or more patterns of neural
stimulation that can be prescribed by a physician and administered
without continuous oversight by a clinical practitioner.
[0060] It is a feature of some embodiments of the invention to meet
one or more of the above-identified objects of the invention using
stimulation systems and methods for chronically stimulating the
pudendal nerve and/or its branches directly, rather than indirectly
by sacral nerve stimulation.
BRIEF DESCRIPTION OF THE DRAWINGS
[0061] The above and other aspects, features and advantages of the
present invention will be more apparent from the following more
particular description thereof, presented in conjunction with the
following drawings wherein:
[0062] FIG. 1 illustrates a programming system for use with an
implantable microstimulator;
[0063] FIG. 2 shows an insertion system for use with an implantable
microstimulator and an exemplary location for the
microstimulator;
[0064] FIG. 3 depicts additional exemplary locations for the
implantable stimulator;
[0065] FIG. 4 illustrates an exemplary embodiment of a stimulation
system of the present invention;
[0066] FIG. 5 illustrates an additional exemplary embodiment of a
stimulation system of the present invention and an exemplary
embodiment of external components of the invention;
[0067] FIG. 6A depicts a preferred approach, according to the
instant invention, for advancing an insertion tool toward the
pudendal nerve;
[0068] FIG. 6B is a partial dissection depicting various bones,
nerves, muscles, and other tissues of the female perineum;
[0069] FIG. 6C is a dissection depicting various bones, nerves,
muscles, vessels, and other tissues of the ischioanal fossa;
and
[0070] FIG. 7 illustrates an additional exemplary embodiment of
external components of the invention.
[0071] Corresponding reference characters indicate corresponding
components throughout the several views of the drawings.
DETAILED DESCRIPTION OF THE INVENTION
[0072] The following description is of the best mode presently
contemplated for carrying out the invention. This description is
not to be taken in a limiting sense, but is made merely for the
purpose of describing the general principles of the invention. The
scope of the invention should be determined with reference to the
claims.
[0073] As indicated above, the present invention reduces or
eliminates incontinence and/or pelvic pain by stimulating various
nerve pathways with various stimulation systems and methods. For
example, the present invention includes a system for using one or
more stimulating drugs and/or electrical stimulation to directly
activate the pudendal nerve and/or its branches by means of an
implantable signal generator and electrode(s) and/or an implantable
pump and catheter(s). One or more electrodes may be surgically
attached to the nerve(s) or implanted adjacent to the nerve(s) to
provide electrical stimulation, and/or one or more catheters may be
surgically attached to the nerve(s) or implanted adjacent to the
nerve(s) to infuse a stimulating drug(s). The stimulating
electrode(s) and/or the infusing catheter(s) may be attached to or
placed adjacent to any part of the pudendal nerve, including a
portion in the pudendal canal and/or any of the distal branches,
such as the dorsal nerve of the penis or clitoris. (As used herein,
"near" and "adjacent" mean as close as reasonably possible to
targeted tissue, including touching or even being positioned within
the tissue, but in general, may be as far as can be reached with
the stimulation pulses.)
[0074] Also, herein, stimulating drugs comprise medications,
anesthetic agents, synthetic or natural hormones,
neurotransmitters, cytokines and other intracellular and
intercellular chemical signals and messengers, and the like. In
addition, certain neurotransmitters, hormones, and other drugs are
excitatory for some tissues, yet are inhibitory to other tissues.
Therefore, where, herein, a drug is referred to as an "excitatory"
drug, this means that the drug is acting in an excitatory manner,
although it may act in an inhibitory manner in other circumstances
and/or locations. Similarly, where an "inhibitory" drug is
mentioned, this drug is acting in an inhibitory manner, although in
other circumstances and/or locations, it may be an "excitatory"
drug. In addition, stimulation of an area herein includes
stimulation of cell bodies and axons in the area.
[0075] When a sensory nerve is stimulated, it produces an
electrical impulse that is transmitted along the axon into the
dorsal horn of the spinal cord, where it can produce perceptible
sensations, modulation of spinal cord circuits, and reflex effects
on motor pathways. When a motor nerve is stimulated, electrical
impulses are conveyed through its many peripheral branches that
supply muscle fibers and elicit contractions in them.
[0076] A preferred stimulation location for purposes of the present
invention is the pelvic floor. Direct stimulation of the pelvic
floor nerves bypasses the potential recruitment of other unrelated
nerve groups at the sacral roots. Nerves in this region that may be
targeted for stimulation include the pudendal nerve, pelvic nerve,
and branches of the pudendal nerve.
[0077] The pudendal nerve and its branches are somatic nerves that
originate from the sacral nerve roots S2, S3, and S4. These and
other somatic nerves emanating from the sacral nerve roots are
preferably stimulated to treat dysfunctions of perineal structures,
such as urinary and/or bowel incontinence, urgency, frequency,
and/or pain. For instance, stimulation of the urethral branch of
the pudendal nerve may be used to inhibit defecation, thereby
treating fecal incontinence. Additionally or alternatively,
stimulation of the inferior rectal branch of the pudendal nerve,
which innervates the external anal sphincter, may also inhibit
defecation, thereby treating fecal incontinence. Stimulation of
other somatic nerves innervating the rectum and/or colon may treat
constipation, fecal retention, and/or colorectal hypomotility.
Stimulation of one or more other pudendal nerve branches (e.g., the
dorsal nerve of the clitoris/penis) may be used as a treatment of,
e.g., urinary urge incontinence and/or detrusor hyperreflexia.
Stimulation of nerves innervating the urethra and/or detrusor
muscle may treat urinary retention, while stimulation of nerves
innervating the internal and/or external urethral sphincter or
their intramuscular branches may treat urinary stress incontinence.
Stimulation of nerve(s) innervating the clitoris and/or vagina may
treat vaginismus, dyspareunia, anorgasmia, or other female sexual
dysfunction.
[0078] In some embodiments of the present invention, pudendal nerve
stimulation is performed at the pudendal canal, a.k.a. Alcock's
canal, where the nerve hooks around the ischial spine. As will be
evident to those of skill in the art, other locations along the
pudendal nerve, and along its branches, may also/alternatively be
stimulated. The location of the pudendal canal may be readily
discerned by a physician, as the ischial spine may be palpated
transvaginally in most patients. A stimulation device may thus be
guided to this area using the ischial spine as a landmark. As
described in more detail presently, such a device may be introduced
transvaginally or transperineally, or via other approaches, such as
transrectally, that will be readily apparent to those skilled in
the art upon reading the present disclosure. The ischial spine may
also be visualized via diagnostic imaging, e.g., CT scan, and such
imaging may be used to guide an electrode(s) to the ischial spine
and thus a targeted location, e.g., the pudendal canal.
[0079] As mentioned above, distal branches of the pudendal nerve
lead, e.g., to the anal sphincter, the perineum, the urethral
sphincter, the penis (in men), the vagina (in women), the glans
penis (in men), and the clitoris (in women). Branches of the
pudendal nerve may be easily accessed percutaneously, and as
described earlier, selective stimulation of a given branch(es) may
offer advantages for the treatment of certain disorders. An
advantage of directly stimulating the pudendal nerve and/or its
branches is the resulting recruitment of sacral nerves S2, S3, and
S4. In addition, the stimulation of the present invention leads to
less side effects than, e.g., sacral nerve stimulation. For
instance, stimulating the pudendal nerve and/or its branches avoids
recruitment of nerves unrelated to the desired treatment, such as
the sciatic nerve.
[0080] Another preferred stimulation location for purposes of the
present invention is the tibial nerve. The tibial nerve is
relatively easily accessible (i.e., relatively near the overlying
skin with no muscle between the nerve and the skin) at two sites in
the leg: at the level of the ankle, immediately posterior to the
medial malleolus and posterior tibial artery and vein; and at the
level of the knee, in the popliteal fossa (i.e., the back of the
knee), immediately lateral to the popliteal artery and vein. Other
sites along the tibial nerve, although not as easily accessible,
are acceptable stimulation sites. Unilateral or bilateral
stimulation is possible. For instance, a microstimulator may be
implanted unilaterally, or two or more microstimulators may be
implanted bilaterally.
[0081] If electrical stimulation is applied by a stimulator, the
electrodes may be configured on one or more leads attached to an
implantable pulse generator (IPG), as described in more detail
presently, or the stimulator may be configured as a
microstimulator, such as described below. Similarly, a drug
infusion system may be included as part of the electrical
stimulator or in a separate stimulator with a reservoir and one or
more catheters for infusion, or alternatively a stimulator may
comprise a microstimulator with a self-contained microinfusion pump
that delivers the drug(s).
[0082] Some embodiments of the present invention utilize one or
more implantable microstimulators. Some microstimulators used with
the present invention are preferably of the type referred to as
BION.RTM. devices, while other small stimulators may alternatively
be used with the present invention. The following documents
describe various features and details associated with the
manufacture, operation and use of BION microstimulators, and are
all incorporated herein by reference:
1 Application/Patent/ Filing/Publi- Publication No. cation Date
Title U.S. Pat. No. 5,193,539 Issued Implantable Microstimulator
Mar 16, 1993 U.S. Pat. No. 5,193,540 Issued Structure and Method of
Mar 16, 1993 Manufacture of an Implantable Microstimulator U.S.
Pat. No. 5,312,439 Issued Implantable Device Having an May 17, 1994
Electrolytic Storage Electrode U.S. Pat. No. 5,324,316 Issued
Implantable Microstimulator June 28, 1994 U.S. Pat. No. 5,405,367
Issued Structure and Method of April 11, 1995 Manufacture of an
Implantable Microstimulator PCT Publication published
Battery-Powered Patient WO 98/37926 Sept 3, 1998 Implantable Device
PCT Publication published System of Implantable WO 98/43700 Oct 8,
1998 Devices For Monitoring and/or Affecting Body Parameters PCT
Publication pubiished System of Implantable WO 98/43701 Oct 8, 1998
Devices For Monitoring and/or Affecting Body Parameters U.S. Pat.
No. 6,051,017 Issued Improved Implantable (application Ser. No.
April 18, 2000 Microstimulator and Systems 09/077,662) Employing
Same published Micromodular Implants to Sept, 1997 Provide
Electrical Stimulation of Paralyzed Muscles and Limbs, by Cameron,
et al., IEEE Transactions on Biomedical Engineering, Vol. 44, No.
9, pages 781-790.
[0083] A microstimulator, when used, is preferably implanted with a
surgical insertion tool specially designed for the purpose, or is
injected (e.g., via a 12 gauge hypodermic needle, or similar
device), in or around nerves and muscles. Alternatively, the device
may be implanted via conventional, endoscopic, or laparoscopic
surgical techniques. Advantageously, the small size of the
microstimulators referenced above permits insertion of these
devices beneath the skin of the perineum, for instance, where they
have the capability to stimulate the nerves and muscles in regions
surrounding the urethra and anus. A more complicated surgical
procedure may be required for fixing the neurostimulator in
place.
[0084] The microstimulators of the type described in the referenced
patents and patent publications represent a new class of generic
implantable stimulators. While each microstimulator is a single
programmable unit, the same external unit may control up to 256
stimulators that then work in harmonious combination to create a
neuromuscular control network. Because the microstimulators are
injectable, they are minimally invasive, and are preferably
injected in an outpatient environment posing little clinical risk,
and reducing costs. If necessary, such microstimulators may be
removed through a small surgical incision.
[0085] In one preferred embodiment, the microstimulator configured
for electrical stimulation comprises two, leadless electrodes.
However, either or both electrodes may alternatively be located at
the ends of short, flexible leads as described in U.S. patent
application Ser. No. 09/624,130, filed Jul. 24, 2000, which is
incorporated herein by reference in its entirety. The use of such
leads may permit electrical stimulation to be directed more locally
to targeted tissue(s) a short distance from the surgical fixation
of the bulk of the implantable stimulator, while allowing most
elements of the microstimulator to be located in a more surgically
convenient site. This minimizes the distance traversed and the
surgical planes crossed by the device and any lead(s). In a
preferred embodiment, the leads are no longer than about 100 to 120
mm.
[0086] For some patients, use of a stimulator for only a few hours
per day or week will improve the symptomatology of incontinence
and/or pelvic pain. In such patients, radio-frequency (RF)
controlled devices provide an adequate amount of stimulation if
used intermittently, e.g., for only a few hours per day, to greatly
decrease the incidence of incontinent and/or painful episodes. For
many other patients, however, a continuous or intermittent
stimulation throughout the day is needed. These patients may best
utilize a stimulator that has a self-contained power source
sufficient to deliver repeated pulses for several hours and that
can be recharged repeatedly, if necessary. In accordance with the
teachings of the present invention, the use of a stimulator with a
rechargeable battery thus provides these patients the portability
needed to free the patient from reliance on RF power delivery.
[0087] A battery-powered microstimulator suitable for use with the
present invention, and a control system for use with such
battery-powered microstimulator, is fully described in earlier
referenced WO 98/37926, published Sep. 3, 1998; WO 98/43700,
published Oct. 8, 1998; and WO 98/43701, published Oct. 8, 1998.
Other microstimulators are suitable for use with the present
invention, such as a microstimulator with a self-contained
microinfusion pump for delivering drug(s). Additional electrical
and drug infusion stimulator systems and methods suitable for use
with the present invention are described herein.
[0088] For purposes of this patent application, it is sufficient to
note that RF controlled stimulators receive power and control
signals from an extra corporeal antenna coil via inductive coupling
of a modulated RF field. Battery-operated stimulators incorporate a
power source within the device itself but rely on RF control,
inductive linking, or the like to program stimulus sequences and to
recharge the power source, when needed. In accordance with the
present invention, each implanted stimulator may be commanded to
produce an electrical and/or infusion pulse of a prescribed
magnitude and duration and at a repetition rate sufficient to cause
stimulation of nerve axons.
[0089] Turning to FIG. 1, a preferred embodiment of the invention
is illustrated. A rechargeable, battery-powered microstimulator 10
is implanted under the skin 6, into subcutaneous region 2, where
current pulses delivered from its electrodes 14 and 16 stimulate
nerve fibers 8. Nerve bundles in the subcutaneous region may carry
somatic sensory axons supplying receptors in skin and muscle and
somatic motor axons supplying skeletal muscle, as well as autonomic
axons supplying visceral and glandular structures and smooth
muscle.
[0090] Microstimulator 10, and all stimulators configured in
accordance with the present invention (e.g., see FIG. 5),
preferably contains electronic circuitry 12 for receiving data
and/or power from outside the body by inductive, RF, or other
electromagnetic coupling. In a preferred embodiment, electronic
circuitry 12 includes an inductive coil for receiving and
transmitting RF data and/or power, an integrated circuit (IC) chip
for decoding and storing stimulation parameters and generating
stimulation pulses (either intermittent or continuous), and
additional discrete electronic components that may be required to
complete the electronic circuit functions, e.g., capacitor(s),
resistor(s), coil(s), and the like.
[0091] Electronic circuitry 12 dictates the amplitude and duration
of the electrical current pulse, when used, thereby determining the
number of nerve fibers excited by each pulse. Advantageously,
electronic circuitry 12 includes a programmable memory 18 for
storing a set(s) of data, stimulation, and control parameters. This
feature allows electrical and/or drug stimulation to be adjusted to
settings that are safe and efficacious with minimal discomfort for
each individual. Specific parameters may provide therapeutic
advantages for various levels and types of incontinence and/or
pain. For instance, some patients may respond favorably to
intermittent stimulation, while others may require continuous
treatment for relief. Electrical and drug stimulation parameters
are preferably controlled independently. However, in some
instances, they are advantageously coupled, e.g., electrical
stimulation may be programmed to occur only during drug
infusion.
[0092] Preferred implantable stimulators also include a power
source and/or power storage device 15. Possible power options for a
stimulation device(s) of the present invention, described in more
detail below, include but are not limited to an external power
source coupled to the stimulation device, e.g., via an RF link, a
self-contained power source utilizing any means of generation or
storage of energy (e.g., a primary battery, a replenishable or
rechargeable battery such as a lithium ion battery, an electrolytic
capacitor, or a super- or ultra-capacitor), and if the
self-contained power source is replenishable or rechargeable, means
of replenishable or recharging the power source (e.g., an RF
link).
[0093] In a preferred embodiment illustrated in FIG. 1, electronic
circuitry 12 receives operating power, recharge power for the
battery (if a rechargeable battery is included within the
stimulator), and data to be stored in memory element 18 by
inductive coupling from external controller 20 and its associated
antenna coil 22. During an initial programming session after
implantation of stimulator 10, the prescribing physician uses a
programming station 30 to download a pattern of stimulus pulse
delivery to controller 20, which saves the information in
nonvolatile memory. Each time stimulator(s) 10 are recharged by
controller 20, the stimulation parameters required from each
stimulator 10 are transmitted via coil 22, along with the power
required for recharging. The stimulation parameters are stored in
memory element 18 of each stimulator 10 as long as power storage
device 15 has sufficient power to operate the stimulator
circuitry.
[0094] According to the preferred embodiment of FIG. 1, program
delivery is initiated by start and stop commands delivered by
patient-governed control switch 26. In this and other preferred
embodiments, controller 20 is a module, preferably handheld,
containing a microprocessor and appropriate nonvolatile memory,
such as electronically erasable programmable read-only-memory
(EEPROM). In additional preferred embodiments, controller 20
operates to control implantable stimulator 10 by any of various
means, including sensing the proximity of a permanent magnet
located in controller 20, or sensing RF transmissions from
controller 20. However, it will be evident to those of skill in
electronic circuitry and computing that many different system
architectures and components could be used to achieve similar
functionality with either a battery-powered or RF-powered
microstimulator device.
[0095] In accordance with one embodiment of the present invention,
a microstimulator is injected into soft tissues by using an
insertion device such as is shown in FIG. 2. The hollow cannula 110
of the insertion device is comprised of a stiff, dielectric
material with sufficient lubricity to permit the undamaged passage
of device 10 therethrough. Probe 120 is a rigid, electrically
conductive trocar whose sharply pointed end extends beyond the end
of the tube. The trocar is used to deliver electrical impulses to
the tissue at its end. Electrical stimuli can be delivered by means
of the trocar 120 by connecting an electrical stimulator (not
shown) to connector 122 on the trocar. The initial insertion site
of the trocar, guided by a clinical knowledge of tissue landmarks
or radiographic images, may be modified until stimulation produces
excitation of nerves 8 judged by perceptible sensations or clinical
demonstration of desired effects on bladder, periurethral muscle or
other pelvic floor musculature. Satisfactory stimulation of nerves
8 will ensure that the end of the rod around the trocar is located
in an appropriate site sufficiently close to nerves 8 so that
electrical stimulation using the microstimulator will also produce
the desired nerve excitation. Insertion of the microstimulator is
accomplished by removing trocar 120 and passing the microstimulator
through the hollow cannula 110 using, e.g., a blunt-ended push-rod
130.
[0096] As mentioned earlier and as depicted in FIG. 3, another
preferred stimulation location for purposes of the present
invention is on or adjacent the tibial nerve 140. The tibial nerve
is relatively easily accessible (i.e., relatively near the
overlying skin with no muscle between the nerve and the skin) at
two sites in the leg. The first is at the level of the ankle,
immediately posterior to the medial malleolus 144, the posterior
tibial artery 146, and the posterior tibial vein 148. The second is
at the level of the knee, in the popliteal fossa (i.e., the back of
the knee), immediately lateral to the popliteal artery 152 and the
popliteal vein 154. Other sites along tibial nerve 140, although
not as easily accessible, are acceptable stimulator locations.
[0097] As depicted in FIG. 4, a preferred microstimulator 10
includes a narrow, elongated capsule 11 containing electronic
circuitry 12 connected to electrodes 14 and 16, which pass through
the walls of the capsule at either end. As detailed in the
referenced patents, electrodes 14 and 16 comprise a stimulating
electrode (to be placed close to the nerve) and an indifferent
electrode (for completing the circuit). Other configurations of
microstimulator 10 are possible, as is evident from the
above-referenced patents.
[0098] The preferred microstimulator 10 should be sufficiently
small to permit its placement near the structures to be stimulated.
Capsule 11 preferably has a diameter no greater than about 3-4 mm,
and more preferably only about 1.5 mm. Capsule length is preferably
no greater than about 20-25 mm, and more preferably only about
10-12 mm. The shape of the microstimulator is preferably determined
by the structure of the desired target, the surrounding area, and
the method of surgical insertion. A thin, elongated cylinder with
electrodes at the ends, as shown in FIG. 4, is currently preferred,
but other shapes, such as spheres, disks or helical structures, are
possible.
[0099] The external surfaces of, e.g., stimulator 10 are
advantageously composed of biocompatible materials. For instance,
capsule 11 is preferably made of, e.g., glass, ceramic, or other
material that provides a hermetic package that will exclude water
vapor but permit passage of electromagnetic fields used to transmit
data and/or power. Stimulating electrodes are preferably made of a
noble or refractory metal or compound, such as platinum, iridium,
tantalum, titanium, titanium nitride, niobium, or alloys of any of
these, in order to avoid corrosion or electrolysis which could
damage the surrounding tissues and/or the device.
[0100] As mentioned earlier, stimulation is provided in accordance
with the teachings of the present invention by electrical
stimulation and/or a stimulating drug(s). The invention includes
one or more stimulators. In the case of electrical stimulation
only, preferred stimulators include a microstimulator(s) and/or an
implantable pulse/signal generator (IPG). In the case of drug
infusion only, preferred stimulators include an implantable pump or
a microstimulator comprising a microinfusion pump. In cases
requiring both electrical stimulation and drug infusion, one or
more stimulators are used. Alternatively and preferably, when
needed, a stimulator provides both electrical stimulation and one
or more stimulating drugs.
[0101] Stimulator 100, depicted in FIG. 5, is preferably implanted
in a surgically-created shallow pocket remote from the stimulation
site, such as in the thigh or flank, more preferably in the
buttocks, and most preferably in the abdomen. Stimulator 100
preferably conforms to the profile of surrounding tissue(s) and/or
bone(s), and is small and compact. This is preferable so that no
unnecessary pressure is applied to the surrounding tissues or skin,
as this may result in skin erosion or infection. Stimulator 100
preferably has a diameter of no greater than 75 mm, more preferably
no greater than 65 mm, and most preferably about 35-55 mm.
Stimulator thickness of approximately 10-12 mm is preferred, while
a thickness of about 8-10 mm or less is more preferred.
[0102] One or more electrode leads 70 and/or catheters 80 attached
to stimulator 100 run subcutaneously, preferably in a
surgically-created tunnel(s), to the tissues to be stimulated. As
previously mentioned, sacral nerve stimulation has commonly been
used to recruit the pudendal nerve and/or its branches, while the
present invention teaches systems and methods for direct, chronic
stimulation of these nerves with a fully implanted stimulator.
[0103] One approach for implantation of a lead(s) and/or
catheter(s) at the pudendal nerve and/or its branches is herein
referred to as the perineal approach. In the following steps,
placement of the electrodes on a lead or of the discharge (end)
portion of a catheter is stated simply as placement of a lead or
catheter. As mentioned earlier, described in more detail below, and
as seen in FIG. 6A, the ischial spine 160 may be used as a landmark
for locating the pudendal nerve, as may the ischial tuberosity 161
(visible in FIGS. 6A, 6B, and 6C). The perineal approach for a
female patient preferably involves the following steps.
[0104] 1. Locate the ischial tuberosity (IT) 161 through the skin.
As best seen in FIG. 6C, a portion of IT 161 lies close to the
surface of the skin.
[0105] 2. Mark the skin 1-5 mm medial from IT 161. This defines the
site 162 for inserting a tool 163 for lead/catheter placement.
[0106] 3. As depicted in FIG. 6A, locate the ischial spine (IS) 160
by inserting one or two fingers into the vagina (or anus) and
palpating laterally (a procedure known in the medical arts). The
pudendal nerve 164 in the pudendal canal 167 (FIG. 6C) lies
adjacent to IS 160.
[0107] 4. Guide the insertion tool 163 toward IS 160. Use finger
pressure against the vaginal (or anal) wall to track insertion of
tool 163 from the marked insertion site 162 toward IS 160.
[0108] 5. Using techniques known in the art, optionally perform
test stimulation to confirm proper lead and/or catheter location,
to confirm response, and/or to determine preliminary stimulator
settings. (This test stimulation may be referred to as an acute
trial, an operating room trial, or a procedure room trial, and may
last from minutes to hours.) For instance, the insertion tool may
include a tip electrode, or electrodes of a lead inserted through
the tool, or drugs delivered through a catheter may be used to
deliver stimulation while analyzing patient response.
Alternatively, a Chalgren 23 gauge, 137 mm long Teflon.TM.
monopolar needle electrode (available from Jari Electrode Supply of
Gilroy, Calif.), or the like, may be used. Response(s) may include
patient report of sensation, vaginal EMG, urethral sphincter PeNTML
and/or anal sphincter PNTML, or other methods known in the art.
[0109] 6. Once at the desired location, deposit the lead and/or
catheter. Depending on the type of tool and lead/catheter used,
this may include pushing the lead/catheter out a cannula, and/or
expelling a biocompatible adhesive to help secure the lead/catheter
to surrounding tissue, and/or expelling a lead/catheter with
self-securing barbs, and/or securing the lead/catheter with an
anchor, sutures, or the like to subcutaneous muscle 165 (FIG. 6B),
fascia 166 (FIG. 6C), or other tissue within an incision at the
insertion site or anywhere along the lead/catheter path, or via
other methods known in the art.
[0110] 7. Once the lead/catheter is deposited and/or anchored,
again optionally perform test stimulation to confirm the
lead/catheter has not shifted out of position. Repeat any steps
required to reposition the lead/catheter.
[0111] 8. If not removed while securing the lead/catheter, remove
tool 163.
[0112] One additional approach for implantation of a lead(s) and/or
catheter(s) at the pudendal nerve and/or its branches, as mentioned
earlier, is herein referred to as the vaginal approach, which
preferably involves the following steps.
[0113] 1. Optionally, grossly locate pudendal nerve 164 in the
pudendal canal by inserting one or two fingers into the vagina and
palpating laterally to locate IS 160.
[0114] 2. Insert a speculum into the vagina.
[0115] 3. With the speculum inserted, again, optionally, grossly
locate pudendal nerve 164 in the pudendal canal by inserting one or
two fingers into the vagina and palpating laterally to locate IS
160.
[0116] 4. Guide the insertion tool 163 through the vaginal wall and
toward IS 160.
[0117] 5. Using techniques known in the art, optionally perform
test stimulation to confirm proper lead and/or catheter location,
to confirm response, and/or to determine preliminary stimulator
settings, as described above.
[0118] 6. Once at the desired location, deposit the lead and/or
catheter, as described above. The lead/catheter may be fixed in
place as described earlier, or by anchoring to tissue exposed
through an incision made in the vaginal wall.
[0119] 7. Once the lead/catheter is deposited and/or anchored,
again optionally perform test stimulation to confirm the
lead/catheter has not shifted out of position. Repeat any steps
required to reposition the lead/catheter.
[0120] 8. If not removed while securing the lead/catheter, remove
the speculum and tool 163.
[0121] Once the electrodes of the lead(s) and/or catheter end
portion(s) are in place, a lead/catheter tunnel(s) will be made,
either to a stimulator implantation site, or possibly to a
percutaneous trial exit site if a percutaneous trial is conducted
prior to implanting a chronic stimulator. A trial period will more
likely be used with patients being treated for pain, but may also
be used with patients being treated for incontinence. To tunnel to
a percutaneous trial exit site, the following steps are
preferred:
[0122] 1. Locate and mark the percutaneous trial exit site. Various
locations are adequate, but a site that is contralateral and
symmetrical to the planned stimulator implant site is
preferred.
[0123] 2. Either run a tunneling tool from the lead/catheter
implantation site to the marked percutaneous trial exit site or run
a tunneling tool from the marked percutaneous trial exit site to
the lead/catheter implantation site. In either case, the tunnel
should be subcutaneous (i.e., just under the skin), or in some
cases, may be deeper. If necessary, an incision(s) may be made to
tunnel in sections, as may be needed if a lead/catheter
extension(s) is used. Tunneling to/from the pudendal nerve and its
branches is new, however, the tunneling tools and methods known in
the art may be adapted for this use.
[0124] 3. Using techniques known in the art, pull
lead(s)/catheter(s)/exte- nsion(s) through the tunnel or tunnel
sections. As appropriate, connect any extension(s) to the implanted
catheter/lead. The lead(s)/catheter(s)/extension(s) may be pulled
either from the lead/catheter implantation site or from the
percutaneous trial exit site. For trial stimulation, it is
preferable, but not required, that a percutaneous extension be
pulled from the exit site to the lead/catheter implantation site,
where the extension is connected to the implanted catheter/lead.
(When trial stimulation is complete, the connector may be cut off
the percutaneous extension so the extension can be pulled back
through the percutaneous exit site to reduce infection risk.) The
proximal end of the lead(s)/catheter(s)/extension(s) (which
attaches to the trial stimulator) should extend from the marked
percutaneous trial exit site.
[0125] 4. Attach the proximal end of the
lead(s)/catheter(s)/extension(s) to the trial stimulator.
[0126] 5. Optionally perform test stimulation to confirm proper
lead and/or catheter location, proper trial stimulator function,
and/or to determine preliminary stimulator settings. Again,
response(s) may include patient report of sensation, vaginal EMG,
urethral sphincter PeNTML and/or anal sphincter PNTML, or other
methods known in the art.
[0127] 6. Surgically close the skin at the lead/catheter
implantation site and around the lead/catheter/extension at the
percutaneous trial exit site, using techniques known in the
art.
[0128] To tunnel to a stimulator site and implant the stimulator,
the following steps are preferred:
[0129] 1. Locate and mark the stimulator implantation site.
[0130] 2. Either run a tunneling tool(s) from the lead/catheter
implantation site to the marked stimulator implantation site or
make an incision at the stimulator implantation site and run a
tunneling tool(s) from the incision to the lead/catheter
implantation site. In either case, the tunnel(s) should be
subcutaneous, or in some cases, may be deeper. If necessary, an
additional incision(s) may be made to tunnel in sections, as may be
needed if a lead/catheter extension(s) is used. Again, tunneling
to/from the pudendal nerve and its branches is new, however, the
tunneling tools and methods known in the art may be adapted for
this use.
[0131] 3. Using techniques known in the art, pull
lead(s)/catheter(s)/exte- nsion(s) through the tunnel or tunnel
sections. As appropriate, connect any extension(s) to the implanted
catheter/lead. The lead(s)/catheter(s)/extension(s) may be pulled
either toward the lead/catheter implantation site or toward the
stimulator implantation site until the proximal end of the
lead(s)/catheter(s)/extension(s) (which attaches to the stimulator)
extends from the marked stimulator implantation site.
[0132] 4. Attach the proximal end of the
lead(s)/catheter(s)/extension(s) to the stimulator.
[0133] 5. Optionally perform test stimulation to confirm proper
lead and/or catheter location, proper stimulator function, and/or
to determine preliminary stimulator settings. Again, response(s)
may include patient report of sensation, vaginal EMG, urethral
sphincter PeNTML and/or anal sphincter PNTML, or other methods
known in the art.
[0134] 6. Implant the stimulator using standard techniques known in
the art.
[0135] 7. Surgically close the skin at the stimulator implantation
site and at the lead/catheter implantation site, using techniques
known in the art.
[0136] Referring again to FIG. 5, in the case of treatment with
electrical stimulation, electrode(s) 72 are carried on lead 70
having a proximal end coupled to stimulator 100. Electrode(s) 72
may include a tip electrode and may include one or more ring
electrodes, allowing bipolar stimulation and/or compensation for
any migration of lead 70. The lead contains wires electrically
connecting electrodes 72 to stimulator 100. Stimulator 100 contains
electrical components 12 that produce electrical stimulation pulses
that travel through the wires of lead 70 and are delivered to
electrodes 72, and thus to the tissue surrounding electrodes 72. To
protect the electrical components inside stimulator 100, the case
of the stimulator is preferably hermetically sealed, as discussed
earlier. For additional protection against, e.g. impact, the case
is preferably made of metal (e.g. titanium) or ceramic, which
materials are also, advantageously, biocompatible. In addition,
stimulator 100 is preferably Magnetic Resonance Imaging (MRI)
compatible.
[0137] In the case of treatment alternatively or additionally
constituting drug infusion, and as illustrated in FIG. 5,
catheter(s) 80 are coupled at a proximal end to stimulator 100,
which contains at least one pump 65 for storing and dispensing one
or more drug(s) through the catheter(s) 80. At and/or along a
distal end, catheter 80 has at least one discharge portion 82 for
infusing dosages of the one or more drugs into a predetermined site
in the brain tissue.
[0138] In one preferred embodiment, shown in FIG. 5, stimulator 100
includes a rechargeable battery as a power source/storage device
15. The battery is recharged, as required, from an external battery
charging system (EBCS) 92, typically through an inductive link 94.
In this embodiment, stimulator 100 includes a processor and other
electronic circuitry 12 that allow it to generate
electrical/infusion pulses that are applied to the patient through
electrodes 72 and/or catheter(s) 80 in accordance with a program
stored in programmable memory 18.
[0139] According to one preferred embodiment of the invention, such
as depicted in FIG. 5, at least one lead 70 is attached to
stimulator 100 via a suitable connector(s) 68, if necessary. Each
lead includes at least two electrodes 72, and may include as many
as sixteen or more electrodes 72. Additional leads 70' and/or
catheter(s) 80' may be attached to stimulator 100. Hence, FIG. 5
shows (in phantom lines) a second catheter 80', and a second lead
70', having electrodes 72' thereon, also attached to stimulator
100.
[0140] Lead(s) 70 are preferably less than 5 mm in diameter, and
more preferably less than 1.5 mm in diameter. Electrodes 72, 72'
are preferably arranged as an array, more preferably are at least
two collinear electrodes, and more preferably at least 4 collinear
electrodes. Stimulator 100 is preferably programmable to produce
either monopolar electrical stimulation, e.g., using the stimulator
case as an indifferent electrode, or bipolar electrical
stimulation, e.g., using one of the electrodes of the electrode
array as an indifferent electrode. A preferred stimulator 100 has
at least four channels and drives up to sixteen electrodes or
more.
[0141] In one preferred embodiment, stimulator 100 of the present
invention is activated and deactivated, programmed and tested
through a hand held programmer (HHP) 101 (which may also be
referred to as a patient programmer and is preferably, but not
necessarily, hand held), a clinician programming system (CPS) 102
(which may also be hand held), or a manufacturing and diagnostic
system (MDS) 103 (which may also be hand held). HHP 101 may be
coupled to stimulator 100 via an RF link 95. Similarly, MDS 103 may
be coupled to stimulator 100 via another RF link 96. In a like
manner, CPS 102 may be coupled to HHP 101 via an infra-red link 97;
and MDS 103 may be coupled to HHP 101 via another infra-red link
98. Other types of telecommunicative links, other than RF or
infra-red may also be used for these purposes. Through these links,
CPS 102, for example, may be coupled through HHP 101 to stimulator
100 for programming or diagnostic purposes. MDS 103 may also be
coupled to stimulator 100, either directly through RF link 96, or
indirectly through the IR link 98, HHP 101, and RF link 95.
[0142] For example, the electrical and/or drug stimulation can
increase the activity of the pudendal afferents, thereby modulating
the activity of the lower urinary tract via reflexive mechanisms
and/or can increase the activity of the pudendal afferents, thereby
acting to increase the tone of the urethral and/or anal sphincter.
Such excitatory stimulation is likely to be produced by
low-frequency electrical stimulation, an excitatory
neurotransmitter agonist(s) (e.g., acetylcholine), an inhibitory
neurotransmitter antagonist(s), a neural depolarizing agent, or any
other drug that acts to cause a portion of an axon to generate an
action potential.
[0143] Electrical stimulation parameters of, for instance, the
pudendal nerve and other somatic nerves emanating from a sacral
root will generally fall in the following ranges:
[0144] Frequency: 2-20 pulses per second (pps).
[0145] Duration: 50-350 microseconds (.mu.s).
[0146] Amplitude: 1-5 volts at about 1-50 milliamps (mA).
[0147] It is to be understood that the above ranges are not
absolute. Rather, they provide a guide for the stimulation
parameters to be used. One of the attractive features provided by
the invention is that the stimulation parameters are programmable
and can be adjusted, as required, until an appropriate and
efficacious stimulation regime is achieved.
[0148] Once again, stimulation and control parameters may be
adjusted to levels that are safe and efficacious and cause the
least discomfort, and parameters may also be chosen to target
specific neural populations and to exclude others, or to increase
neural activity in specific neural populations and to decrease
neural activity in others. For example, relatively low frequency
neurostimulation (i.e., less than about 50-100 Hz) typically has an
excitatory effect on surrounding neural tissue, leading to
increased neural activity, whereas relatively high frequency
neurostimulation (i.e., greater than about 50-100 Hz) typically has
an inhibitory effect, leading to decreased neural activity.
Similarly, excitatory neurotransmitters (e.g., acetylcholine)
agonists thereof, and agents that act to increase levels of an
excitatory neurotransmitter(s) (e.g., edrophonium) generally have
an excitatory effect on neural tissue, while inhibitory
neurotransmitters (e.g., gamma-aminobutyric acid, a.k.a. GABA),
generally have an inhibitory effect. However, antagonists of
inhibitory neurotransmitters (e.g., bicuculline) and agents that
act to decrease levels of an inhibitory neurotransmitter(s) have
been demonstrated to excite neural tissue, leading to increased
neural activity.
[0149] For example, somatic nerves that originate from S2, S3, and
S4 nerve roots, e.g. the pudendal nerve and its nerve branches, may
be stimulated to treat incontinence, urgency, frequency, and/or
pelvic pain. In one alternative, exciting the urethral branch of
the pudendal nerve will inhibit defecation in some patients.
Low-frequency electrical stimulation (e.g., less than about 50-100
Hz) and/or infusion of, e.g., acetylcholine, is likely to produce
such excitement. In another alternative, exciting other branches of
the pudendal nerve, especially the dorsal nerve of the clitoris in
the female and the dorsal nerve of the penis in the male, will
prevent urination and/or defecation in some patients. Once again,
low-frequency stimulation and/or infusion of, e.g., acetylcholine,
is likely to provide this excitement.
[0150] In another alternative, exciting the pudendal nerve at the
point where it passes through the pudendal canal (a.k.a. Alcock's
Canal) will prevent urination and/or defecation and/or will control
pelvic pain in some patients. Once again, low-frequency stimulation
and/or infusion of, e.g., acetylcholine, is likely to provide this
excitement.
[0151] As a further example, large diameter fibers (e.g., A-.alpha.
and/or A-.beta. fibers) respond to relatively lower current density
stimulation compared with small diameter fibers (e.g., A-.delta.
and/or C fibers). Typically, relatively large diameter nerve fibers
respond to pressure and light touch, while smaller fibers respond
to pain. For example, stimulation of the pudendal nerve with
relatively low current density may cause relatively non-painful
(e.g., tingling) sensations that may treat incontinence in some
patients.
[0152] Advantageously, by implanting one or more stimulators in the
manner described herein so as to selectively stimulate appropriate
nerves and/or tissue, it is possible to create a system which: (1)
reduces or eliminates the incidence of unintentional episodes of
bladder or colon emptying by stimulating nerve pathways that
diminish involuntary bladder or colon contractions, (2) improves
closure of the bladder/colon outlet, (3) improves the long-term
health of the urinary system by increasing bladder capacity and
period between emptying and/or (4) reduces or eliminates pelvic
pain.
[0153] According to one embodiment of the invention, a stimulator
operates independently. According to another embodiment of the
invention, a stimulator operates in a coordinated manner with other
stimulator(s), other implanted device(s), or other device(s)
external to the patient's body. For instance, a stimulator may
control or operate under the control of another implanted
stimulator(s), other implanted device(s), or other device(s)
external to the patient's body. A stimulator may communicate with
other implanted stimulators, other implanted devices, and/or
devices external to a patient's body via, e.g., an RF link, an
ultrasonic link, or an optical link. Specifically, a stimulator may
communicate with an external remote control (e.g., patient and/or
physician programmer) that is capable of sending commands and/or
data to a stimulator and that is preferably capable of receiving
commands and/or data from a stimulator.
[0154] In order to help determine the strength and/or duration of
electrical stimulation and/or the amount and/or type(s) of
stimulating drug(s) required to produce the desired therapeutic
effect, in one preferred embodiment, a patient's response to and/or
need for treatment is sensed. For instance, the muscle activity
produced in response to stimulation may be detected, e.g., via
recording of the associated electromyograph (EMG). Thus, when
electrodes and/or catheters of a stimulator are implanted, for
example, near the dorsal nerve of the clitoris (a branch of the
pudendal nerve), the signals from an EMG sensor built into the
stimulator may be used to adjust stimulation parameters.
[0155] Alternatively, a "stimulator" dedicated to sensory processes
communicates with a stimulator that provides the electrical and/or
infusion pulses. For instance, a "microstimulator" may be
introduced into the bladder to sense changes in bladder pressure.
As described below, the implant circuitry 12 may, if necessary,
amplify and transmit these signals, which may be analog or digital.
Other methods of determining the required stimulation include
sensing bladder volume, impedance, absorption of light, sphincter
or colon pressure, muscular activity associated with the sphincter,
bladder, or colon via electromyograph, observing the stimulation
required to decrease or eliminate pain, sensing other measures of
the state of the patient, such as levels or changes of any blood
borne substance, including medications and hormones, and other
methods mentioned herein, and others that will be evident to those
of skill in the art upon review of the present disclosure. The
sensed information is preferably used to control the stimulation
parameters in a closed-loop manner.
[0156] In another preferred embodiment as illustrated in FIG. 7,
using for example, a microstimulator(s), the patient 170 switches
implantable microstimulator 10 on and off by use of controller 180,
which is preferably handheld. Controller 180 operates to control
implantable stimulator 10 by any of various means, including
sensing the proximity of a permanent magnet located in controller
180, or sensing RF transmissions from controller 180.
[0157] External components for one preferred embodiment related to
programming and providing power to stimulator 10 are also
illustrated in FIG. 7. When it is required to communicate with
implanted stimulator 10, patient 170 is positioned on or near
external appliance 190, which appliance contains one or more
inductive coils 192 or other means of communication (e.g., RF
transmitter and receiver). External appliance 190 is connected to
or is a part of external electronic circuitry appliance 200 which
receives power 202 from a conventional power source. External
appliance 200 contains manual input means 208, e.g., a keypad,
whereby the patient 170 or a caregiver 212 may request changes in
the parameters of the electrical and/or drug stimulation produced
during normal operation of implantable stimulator 10. In this
embodiment, manual input means 208 includes various
electromechanical switches and visual display devices that provide
the patient and/or caregiver with information about the status and
prior programming of implantable stimulator 10.
[0158] Alternatively or additionally, external electronic appliance
200 is preferably provided with an electronic interface means 216
for interacting with other computing means 218, such as by a serial
interface cable or infrared link to a personal computer or to a
telephone modem. Such interface means 216 thus permits a clinician
to monitor the status of the implant(s) and prescribe new
stimulation parameters from a remote location.
[0159] The external appliance(s) may advantageously be embedded in
a cushion, mattress cover, or garment. Other possibilities exist,
including a belt, strap, or other structure that may be affixed to
the patient's body or clothing.
[0160] Thus, it is seen that in accordance with the present
invention, one or more external appliances are preferably provided
to interact with the stimulator(s) to accomplish one or more of the
following functions:
[0161] Function 1: If necessary, transmit electrical power from the
external electronic appliance 200 via appliance 190 to stimulator
10 in order to power the device and/or recharge the power
source/storage device 15. External electronic appliance 200 may
include an automatic algorithm that adjusts electrical and/or
stimulation parameters automatically whenever the stimulator(s) 10
is/are recharged.
[0162] Function 2: Transmit data from the external appliance 200
via the external appliance 190 to stimulator 10 in order to change
the parameters of electrical and/or drug stimulation produced by
stimulator 10.
[0163] Function 3: Transmit sensed data indicating a need for
treatment or in response to stimulation (e.g., pressure, neural
activity (e.g., ENG), muscle activity (e.g., EMG), impedance, or
other activity) to external appliance 200 via external appliance
190.
[0164] Function 4: Transmit data indicating state of the stimulator
(e.g., battery level, drug level, electrical stimulation an/or
infusion settings, etc.) to external appliance 200 via external
appliance 190.
[0165] By way of example, a treatment modality for incontinence may
be carried out according to the following sequence of
procedures:
[0166] 1 A first stimulator 10 is implanted so that its electrodes
14 and 16 are located adjacent to nerve fibers 8. A second
stimulator 10 is implanted into the bladder.
[0167] 2 Using Function 2 described above (i.e., transmitting data)
of external electronic appliance 200 and external appliance 190,
the first implantable stimulator 10 is commanded to produce a
series of excitatory electrical stimulation pulses with gradually
increasing amplitude, possibly while infusing gradually increasing
amounts of an excitatory neurotransmitter, e.g., acetylcholine.
[0168] 3. After each stimulation/infusion pulse, or at some other
predefined interval, any change in bladder pressure resulting from
the electrical an/or drug stimulation is sensed by the second
implantable stimulator 10. These responses are converted to data
and telemetered out to the external electronic appliance 200 via
Function 3.
[0169] 4. From the response data received at external appliance 200
from the second implantable stimulator 10, the stimulus threshold
for obtaining a reflex response is determined and is used by a
clinician acting directly 212 or by other computing means 218 to
transmit the desired electrical and/or drug stimulation parameters
to the first implantable stimulator 10 in accordance with Function
2.
[0170] 5. When patient 170 desires to invoke electrical stimulation
and/or drug infusion, patient 170 employs controller 180 to set the
first stimulator 10 in a state where it delivers a prescribed
stimulation pattern from a predetermined range of allowable
stimulation patterns.
[0171] 6. Patient 170 employs handheld controller 180 to turn off
the first stimulator 10, if desired.
[0172] 7. Periodically, the patient or caregiver recharges the
power source/storage device 15 of the first and/or second
implantable stimulator 10, if necessary, in accordance with
Function 1 described above (i.e., transmit electrical power).
[0173] In another example, referring again to FIG. 5, a treatment
modality for incontinence may be carried out according to the
following sequence of procedures:
[0174] 1 A stimulator 100 is implanted in the inner thigh,
buttocks, abdomen, flank, or other remote location, and its lead 70
and/or catheter 80 tunneled so that electrodes 72 and/or catheter
discharge portion 82 are located adjacent to the pudendal nerve 164
at Alcock's canal 167 (FIG. 6C). If necessary or desired,
additional leads 70' and/or catheters 80' may be used so that
additional electrodes 72' and/or catheter discharge portions(s) 82'
may additionally or alternatively be located in or adjacent sacral
nerve roots. Additional electrodes 72' may be implanted, e.g., on
the bladder.
[0175] 2 Using HHP 101 described above, stimulator 100 is commanded
to produce a series of excitatory electrical stimulation pulses
with gradually increasing amplitude, possibly while infusing
gradually increasing amounts of an excitatory neurotransmitter,
e.g., acetylcholine.
[0176] 3. After each stimulation/infusion pulse, or at some other
predefined interval, any change in bladder pressure resulting from
the electrical an/or drug stimulation is sensed by the additional
electrodes 72' implanted on the bladder.
[0177] 4. These responses are converted to data and telemetered out
to HHP 101, and from there, to CPS 102. From the response data
received at CPS 102, the stimulus threshold for obtaining a reflex
response is determined and is used by a clinician using CPS 102
and/or HHP 101 to transmit the desired electrical and/or drug
stimulation parameters to stimulator 100. Alternatively, the
response data are converted to data and used directly by stimulator
100 to modify electrical and/or drug stimulation parameters in a
closed-loop method.
[0178] 5. When patient 170 desires to invoke electrical stimulation
and/or drug infusion, patient 170 employs HHP 101 to set stimulator
100 in a state where it delivers a prescribed stimulation pattern
from a predetermined range of allowable stimulation patterns.
[0179] 6. Patient 170 employs HHP 101 to turn off stimulator 100,
if desired.
[0180] 7. Periodically, the patient or caregiver recharges the
power source/storage device 15 of the stimulator 100, if necessary,
using EBCS 92.
[0181] For the treatment of any of the various types and severities
of incontinence, urgency, frequency, or pelvic pain, it may be
desirable to modify or adjust the algorithmic functions performed
by the implanted and/or external components, as well as the
surgical approaches, in ways that would be obvious to skilled
practitioners of these arts. For example, it may be desirable to
employ more than one implantable stimulator 10, each of which could
be separately controlled by means of a digital address. Multiple
channels and/or multiple patterns of electrical and/or drug
stimulation might thereby be programmed by the clinician and
controlled by the patient in order to deal with complex or multiple
symptoms or dysfunctions such as may occur as a result of spinal
cord injury and neurodegenerative disorders.
[0182] In one preferred embodiment, a stimulator, or a group of two
or more stimulators, is controlled via closed-loop operation. A
need for and/or response to stimulation is sensed by the
stimulator(s), or by an additional "stimulator" (which may or may
not be dedicated to the sensing function), or another implanted or
external device.
[0183] If necessary, the sensed information is transmitted to the
stimulating stimulator(s). Preferably, the parameters used by the
stimulator(s) are automatically adjusted based on the sensed
information. Thus, the electrical and/or drug stimulation
parameters are adjusted in a closed-loop manner to provide
stimulation tailored to the need for and/or response to the
electrical and/or drug stimulation.
[0184] For instance, in one embodiment of the present invention, a
first and second "stimulator" are provided. The second "stimulator"
periodically (e.g. once per minute) records bladder pressure and
transmits it to the first stimulator. The first stimulator uses the
bladder pressure information to adjust electrical and/or drug
stimulation parameters according to an algorithm programmed, e.g.,
by a physician. For example, the amplitude of electrical
stimulation may be increased in response to increased bladder
pressure. More preferably, one stimulator performs both the sensing
and stimulating functions.
[0185] While a stimulator may also incorporate means of sensing
incontinence, urgency, frequency, or pain, e.g., via a pressure
sensor or electromyograph, it may alternatively or additionally be
desirable to use a separate or specialized implantable device to
record and telemeter physiological conditions/responses in order to
adjust electrical stimulation and/or drug infusion parameters. This
information may be transmitted to an external device, such as
external appliance 190, or may be transmitted directly to implanted
stimulator(s). However, in some cases, it may not be necessary or
desirable to include a sensing function or device, in which case
stimulation/infusion parameters are determined and refined, for
instance, by patient feedback.
[0186] While the invention herein disclosed has been described by
means of specific embodiments and applications thereof, numerous
modifications and variations could be made thereto by those skilled
in the art without departing from the scope of the invention set
forth in the claims.
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